Chronic intermittent ethanol and acute stress similarly modulate BNST CRF neuron activity via noradrenergic signaling

BioRxiv : the Preprint Server for Biology
Angela E SnyderYuval Silberman

Abstract

Relapse is a critical barrier to effective long-term treatment of alcoholism, and stress is often cited as a key trigger to relapse. Numerous studies suggest that stress-induced reinstatement to drug seeking behaviors is mediated by norepinephrine (NE) and corticotropin releasing factor (CRF) signaling interactions in the bed nucleus of the stria terminalis (BNST), a brain region critical to many behavioral and physiologic responses to stressors. Here we sought to directly examine the effects of NE on BNST CRF neuron activity and determine if these effects may be modulated by chronic intermittent EtOH (CIE) exposure or a single restraint stress. Utilizing whole-cell patch clamp electrophysiological techniques in CRF-tomato reporter mice, we found that NE depolarized BNST CRF neurons in naive mice in a β-adrenergic receptor (AR) dependent mechanism. CRF neurons from CIE or stress-exposed mice had significantly elevated basal resting membrane potential compared to naive mice. Furthermore, CIE and stress individually disrupted the ability of NE to depolarize CRF neurons, suggesting that both stress and CIE utilize β-AR signaling to modulate BNST CRF neurons. Neither stress nor CIE altered the ability of exogenous NE to inhibit evo...Continue Reading

Related Concepts

Ethanol
Alcoholic Intoxication, Chronic
Brain
Cell Nucleus
Corticotropin-Releasing Hormone
Equilibrium
General Adaptation Syndrome
Laboratory mice
Neurons
Norepinephrine

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